TLR agonists have a strong binding affinity to receptor sites meant to recognize foreign pathogens and this actively boosts immune signaling more than endogenous cell death signals.29,30 After tumor antigen is released and taken up by dendritic cells (DCs), RES further promotes adaptive immune recognition by binding to TLR7 and TLR8 on DCs, stimulating the production of type 1 IFNs and helping to prime and expand the population of tumor-specific CD8+ T cells.31,32. This evidence concerns the gene TLR8 and neoplasm.